We have studied the influence of external potassium and sodium ions on resting and depolarized membrane potentials of sheep Purkinje fibers. After the fibers were exposed to Tyrode's solution containing low external K concentration (1 mM), the following membrane potential changes were observed. The resting membrane potential was first slightly increased for a few minutes and then slowly declined. During the decline, there was a rapid depolarization which was followed by a brief repolarization and then a depolarized stable potential. This depolarized potential was maintained as long as the fibers were exposed to the low K concentration. In some fibers, spontaneous action potentials occurred during the transition from the slow decline to the maintained depolarization. This maintained depolarization may be the potential level of plateau of spontaneous action potentials. Restoration of normal K concentration was followed by a rapid repolarization, a transient hyperpolarization and finally a resting membrane potential. The mean values (plus or minus S.E.) of membrane potential in the resting state, the maintained depolarization and the transient hyperpolarization were 80.5 plus or minus 1.1 mV, 36.1 plus or minus 1.9 mV, and 91.4 plus or minus 2.1 mV, respectively. It was found that the ion responsible for the rapid depolarization and the maintained depolarization is the Na ion. The contribution of external Na ion to membrane potential in the maintained depolarization was increased by 8 times as compared with that in the resting potential, indicating an increase of the relative Na permeability in the depolarized state. Reduction of external Ca concentration retarded the rapid repolarization and diminished the transient hyperpolarization. The mean values (plus or minus S.E.) of intracellular K ion activities were 121.4 plus or minus 2.9 mM in the resting state, 119.7 plus or minus 3.4 mM in the depolarized state, and 119.0 plus or minus 3.7 mM in the transient hyperpolarization which are not significantly different from each other. These results suggest that the transient hyperpolarization may be due to an alteration of extracellular K concentration in the narrow clefts. Application of ouabain diminished the transient hyperpolarization.